scholarly journals Moderate Exercise Combined with Enriched Environment Enhances Learning and Memory through BDNF/TrkB Signaling Pathway in Rats

2021 ◽  
Vol 18 (16) ◽  
pp. 8283
Author(s):  
Liyuan Xu ◽  
Linna Zhu ◽  
Lina Zhu ◽  
Dandan Chen ◽  
Kelong Cai ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Learning And Memory ◽  
Receptor Tyrosine Kinase ◽  
Treadmill Exercise ◽  
Escape Latency ◽  
Enriched Environment ◽  
Enzyme Linked Immunosorbent Assay ◽  
Healthy Male ◽  
Memory Ability ◽  
Male Wistar Rats

This study aimed to investigate the effects and potential mechanisms of exercise combined with an enriched environment on learning and memory in rats. Forty healthy male Wistar rats (7 weeks old) were randomly assigned into 4 groups (N = 10 in each group): control (C) group, treadmill exercise (TE) group, enriched environment (EE) group and the TE + EE group. The Morris water maze (MWM) test was used to evaluate the learning and memory ability in all rats after eight weeks of exposure in the different conditions. Moreover, we employed enzyme-linked immunosorbent assay (ELISA) to determine the expression of brain-derived neurotrophic factor (BDNF) and receptor tyrosine kinase B (TrkB) in the rats. The data showed that the escape latency and the number of platform crossings were significantly better in the TE + EE group compared to the TE, EE or C groups (p < 0.05). In addition, there was upregulation of BDNF and TrkB in rats in the TE + EE group compared to those in the TE, EE or C groups (p < 0.05). Taken together, the data robustly demonstrate that the combination of TE + EE enhances learning and memory ability and upregulates the expression of both BDNF and TrkB in rats. Thus, the BDNF/TrkB signaling pathway might be modulating the effect of exercise and enriched environment in improving learning and memory ability in rats.

scholarly journals DHA supplementation improves behavioral memory impairment and alleviates oxidative stress in hippocampal caused by repeated anesthesia of sevoflurane in aged rats

2020 ◽  
Author(s):  
Ming Tian ◽  
Kezhong Li ◽  
Xiaoling Zhao
Keyword(s):  
Signaling Pathway ◽  
Learning And Memory ◽  
Memory Impairment ◽  
Escape Latency ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Group Model ◽  
Aged Rats ◽  
Sevoflurane Anesthesia ◽  
Behavioral Memory

Abstract Backgroud: The current study aimed to explore the effects of docosahexaenoic acid (DHA) on the behavioral memory impairment induced by repeated anesthesia of sevoflurane in aged rats. Methods: A total of 54 Sprague‑Dawley (SD) aged rats were randomly divided into five groups: Blank control group (Control), sevoflurane group (Model), DHA group (3g/kg), Sev + DHA (0.3g/kg) group, Sev + DHA (1g/kg) group and Sev + DHA (3g/kg) group. Morris water maze experiment was used to evaluate the learning and memory ability. Hematoxylin and eosin (H&E) staining was used to observe histological changes in the hippocampus. Enzyme linked immunosorbent assay (ELISA) was used to detect the content of superoxide dismutase (SOD), malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) in hippocampus. Immunohistochemistry and western blot analysis were used to determine the expression of the Nuclear factor erythroid-2 (NF-E2)-related factor 2(Nrf2)/ hemeoxygenase-1 (HO-1) signaling pathway. Results: Rats were indicated to exhibit prolonged escape latency following sevoflurane anesthesia. The number of times taken to cross the platform and the time for target quadrant stay were also demonstrated to be significantly reduced. Rats treated with different doses of DHA were revealed to exhibit reduced escape latency. The number of times taken to cross the platform and the time for target quadrant stay increased. Histopathological examination indicated that DHA ameliorated the brain function of the rats that were repeatedly anesthetized using sevoflurane. Furthermore, the expression of Nrf2 and HO-1 protein were demonstrated to be significantly increased. Conclusions: The present study revealed that DHA has a protective effect on learning and memory impairment in aged rats induced by repeated sevoflurane anesthesia, and the mechanism may be associated with the Nrf2/HO-1 signaling pathway.

Change of learning and memory ability and IGF-1 level in type 3 diabetes rats and effect of analog P165 of APP 5-mer peptide

2011 ◽  
Vol 26 (S2) ◽  
pp. 503-503
Author(s):  
R. Wang
Keyword(s):  
Learning And Memory ◽  
Escape Latency ◽  
Serum Glucose ◽  
Morris Water Maze Test ◽  
Control Group ◽  
Model Group ◽  
Memory Ability ◽  
Type 3 Diabetes ◽  
Significant Difference ◽  
Type 3

ObjectiveTo investigate the effect of Analog P165 of APP5-mer peptide on change of learning and memory ability in type 3 diabetes rats.MethodHealthy adult male rats were randomly divided into 3 groups: Control group; type 3 diabetes (T3DM) group; T3DM administrated P165 group. T3DM models were induced by intracerebroventricular injection of Streptozotocin (STZ, 3 mg/kg) bilaterally. P165 groups were treated with gastric P165 (355 μg/kg) Then, learning and memory ability was detected by Morris water maze test. Body weight and serum glucose were recorded. The rat serum Insulin, Gluocagon, insulin-like growth factor-1 (IFG-1) was detected by ELISA method.ResultsIn the Morris water maze test, compared with control group, the escape latency increased significantly (p < 0.05) in model group at the 3rd day. Compared with model group, the escape latency decreased significantly (p < 0.05) in the models administrated P165 group at the 3rd day. Although there was no significant difference, the escape latency decreased in P165 group at the 4th and 5th day. From the result of rats blood serum detection, the serum IGF-1 level decreased significantly in the model group (p < 0.01) than the control group. The serum IGF-1 level increased significantly in P165 treated group(p < 0.05).The body weight and the serum glucose, insulin, gluocagon had no significant difference among the groups in the period of experiment.ConclusionThere is learning and memory impairment in the T3DM rats. P165 can raise the rats blood serum IGF-1 level, ameliorate learning and memory ability but don’t influence the serum glucose.

scholarly journals Interventional Effects of DHA on Behavioral Memory Impairment Caused by Repeated Anesthesia of Sevoflurane in Aged Rats

2020 ◽  
Author(s):  
Ming Tian ◽  
Kezhong Li ◽  
Xiaoling Zhao
Keyword(s):  
Signaling Pathway ◽  
Learning And Memory ◽  
Memory Impairment ◽  
Escape Latency ◽  
Control Group ◽  
High Dose ◽  
Group Model ◽  
Aged Rats ◽  
Sevoflurane Anesthesia ◽  
Behavioral Memory

Abstract Backgroud: The current study aimed to explore the effects of Docosahexaenoic acid (DHA) on the behavioral memory impairment induced by repeated anesthesia of sevoflurane in aged rats. Methods: A total of 45 Sprague‑Dawley (SD) aged rats were randomly divided into five groups: Blank control group (Control), sevoflurane group (Model), low-dose DHA group (L-DHA; 0.3g/kg), medium-dose DHA group (M-DHA; 1g/kg) and high-dose DHA group (H-DNA; 3g/kg). Morris water maze experiment was used to evaluate the learning and memory ability of rats. Hematoxylin and eosin staining was used to observe histological changes in the hippocampus. Immunohistochemistry and western blot analysis were used to determine the expression of the Nuclear factor erythroid-2 (NF-E2)-related factor 2(Nrf2)/hemeoxygenase-1 (HO-1) signaling pathway. Results: Rats were indicated to exhibit prolonged escape latency following sevoflurane anesthesia. The number of times taken to cross the platform and the time for target quadrant stay were also demonstrated to be significantly reduced. Rats treated with different doses of DHA were revealed to exhibit reduced escape latency. The number of times taken to cross the platform and the time for target quadrant stay increased. Histopathological examination indicated that DHA attenuated the brain function of the rats that were repeatedly anesthetized using sevoflurane. Furthermore, the expression of Nrf2 and HO-1 protein were demonstrated to be significantly increased. Conclusions: The present study revealed that DHA has a protective effect on learning and memory impairment in aged rats induced by repeated sevoflurane anesthesia, and the mechanism may be associated with the Nrf2/HO-1 signaling pathway.

Neuroprotective effect of miR-204-5p downregulation against isoflurane-induced learning and memory impairment via targeting EphB2 and inhibiting neuroinflammation

2021 ◽  
pp. 096032712110099
Author(s):  
H Liu ◽  
M Wang ◽  
L Xu ◽  
M Li ◽  
M Zhao
Keyword(s):  
Learning And Memory ◽  
Memory Impairment ◽  
Target Genes ◽  
Escape Latency ◽  
Neuroprotective Effect ◽  
Luciferase Reporter ◽  
Enzyme Linked Immunosorbent Assay ◽  
Spatial Learning And Memory ◽  
Protective Effects ◽  
Factor Α

Background: Isoflurane, one of the most commonly used inhalational anesthetics, is usually used in surgery patients and often causes long-term learning and memory impairment. The aim of this study was to explore the role of microRNA-204-5p (miR-204-5p) in isoflurane-induced learning and memory impairment in rats. Methods: The Morris Water Maze (MWM) test was used to estimate the spatial learning and memory abilities of laboratory rats. Enzyme-linked immunosorbent assay (ELISA) was used to determine interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α) concentrations in the hippocampal tissues. The expression level of miR-204-5p was determined by using quantitative reverse transcription polymerase chain reaction (qRT-PCR). The potential target genes of miR-204-5p were predicted and verified by the TargetScan and dual-luciferase reporter assay, respectively. Results: Isoflurane-induced rats showed significantly higher neurological function scores, higher escape latency and shorter time spent in the original quadrant. Isoflurane could significantly induce neuroinflammation, and the expression of miR-204-5p was increased in the hippocampal tissue of rats exposed to isoflurane. Moreover, downregulation of miR-204-5p attenuated the effect of isoflurane treatment on the escape latency and the time in the original quadrant, and inflammatory cytokines level was downregulated by inhibiting the expression of miR-204-5p. EphB2 was verified as a direct target gene of miR-204-5p. Conclusion: Downregulated miR-204-5p exerts protective effects against isoflurane-induced learning and memory impairment via targeting EphB2 and inhibiting neuroinflammation. MiR-204-5p could serve as a potential therapeutic target for the lightening of cognitive dysfunction induced by isoflurane.

scholarly journals Effects of Loofah cylindrica extract on learning and memory ability, brain tissue morphology, and immune function of aging mice

2021 ◽  
Vol 16 (1) ◽  
pp. 399-407
Author(s):  
Limin Dong ◽  
Chunjie Liu
Keyword(s):  
Immune Function ◽  
Learning And Memory ◽  
Brain Tissue ◽  
Ratio Method ◽  
Mouse Serum ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Memory Ability ◽  
Tissue Morphology ◽  
Spleen Index

Abstract In this study, we aimed to observe the effects of Loofah cylindrica (LC) extract on learning and memory ability, brain tissue morphology, and immune function of aging mice. Kunming mice were selected and randomly divided into a control group, a positive control group, an aging group, and three dose groups. Three dose groups were administered 187.5, 375, and 750 mg/kg of LC extract, respectively. Except for the control group, the mice in any other group were continuously subcutaneously injected d-galactose on the back and neck. Platform tests and Morris water maze (MWM) were adopted to test the learning and memory ability of each group. The brain index, thymus index, and spleen index of each group were determined by the organ-to-body ratio method. The enzyme-linked immunosorbent assay was performed to measure the concentration of cytokines interleukin 2 and interferon gamma and the proliferation activity of T lymphocytes in mouse serum. In addition, the hematoxylin and eosin staining was employed to observe the morphological changes in mouse brain tissues of each group. The results show that the aging group made more errors in the platform test, had longer escape latency, shorter swimming time in the platform quadrant, and fewer platform crossings in the MWM; much fewer brain tissue cells; and smaller brain index, thymus index, and spleen index. The LC extracts (375 and 750 mg/kg) can significantly antagonize the changes in the above indices. It can be concluded that LC extract can improve the learning and memory of aging mice, enhance their immune activity, and delay the aging process.

scholarly journals Anti-Inflammatory Effect of Simonsinol on Lipopolysaccharide Stimulated RAW264.7 Cells through Inactivation of NF-κB Signaling Pathway

Molecules ◽  
2020 ◽  
Vol 25 (16) ◽  
pp. 3573
Author(s):  
Lian-Chun Li ◽  
Zheng-Hong Pan ◽  
De-Sheng Ning ◽  
Yu-Xia Fu
Keyword(s):  
Nitric Oxide ◽  
Signaling Pathway ◽  
Morphological Changes ◽  
Raw264.7 Cells ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Oxide Synthase ◽  
Necrosis Factor

Simonsinol is a natural sesqui-neolignan firstly isolated from the bark of Illicium simonsii. In this study, the anti-inflammatory activity of simonsinol was investigated with a lipopolysaccharide (LPS)-stimulated murine macrophages RAW264.7 cells model. The results demonstrated that simonsinol could antagonize the effect of LPS on morphological changes of RAW264.7 cells, and decrease the production of nitric oxide (NO), tumor necrosis factor α (TNF-α), and interleukin 6 (IL-6) in LPS-stimulated RAW264.7 cells, as determined by Griess assay and enzyme-linked immunosorbent assay (ELISA). Furthermore, simonsinol could downregulate transcription of inducible nitric oxide synthase (iNOS), TNF-α, and IL-6 as measured by reverse transcription polymerase chain reaction (RT-PCR), and inhibit phosphorylation of the alpha inhibitor of NF-κB (IκBα) as assayed by Western blot. In conclusion, these data demonstrate that simonsinol could inhibit inflammation response in LPS-stimulated RAW264.7 cells through the inactivation of the nuclear transcription factor kappa-B (NF-κB) signaling pathway.

scholarly journals Anemoside B4 ameliorates TNBS-induced colitis through S100A9/MAPK/NF-κB signaling pathway

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Yong Zhang ◽  
Zhengxia Zha ◽  
Wenhua Shen ◽  
Dan Li ◽  
Naixin Kang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathway ◽  
Tca Cycle ◽  
Mapk Signaling ◽  
Enzyme Linked Immunosorbent Assay ◽  
Trinitrobenzene Sulfonic Acid ◽  
Therapeutic Effects ◽  
Triterpenoid Saponin ◽  
Label Free

Abstract Background Despite the increased morbidity of ulcerative colitis (UC) in the developing countries, available treatments remain unsatisfactory. Therefore, it is urgent to discover more effective therapeutic strategies. Pulsatilla chinensis was widely used for the treatment of inflamed intestinal diseases including UC for thousands of years in China. Anemoside B4, the most abundant triterpenoid saponin isolated from P. chinensis, exerts anti-inflammatory and antioxidant effects and may be the most active compounds, which is responsible for the therapeutic effects. However, the mechanism how anemoside B4 executes its biological functions is still elusive. Methods Here, we used the 2, 4, 6-trinitrobenzene sulfonic acid (TNBS)-induced colitis rat model to evaluate the therapeutic effect of anemoside B4. Blood samples of colitis rats were collected for hematology analysis. The inflammation-associated factors were investigated by enzyme-linked immunosorbent assay (ELISA). Cell proliferation and apoptosis was determined with EdU cell proliferation assay and TUNEL assay. The proteins regulated by anemoside B4 were identified by label-free quantitative proteomics. The significantly down-regulated proteins were verified by Western blotting analysis. mRNA expression was analyzed by quantitative real-time RT-PCR. Results The results showed that anemoside B4 ameliorated TNBS-induced colitis symptoms, including tissue damage, inflammatory cell infiltration, and pro-inflammatory cytokine production, apoptosis and slowed proliferation in colon. Quantitative proteomic analyses discovered that 56 proteins were significantly altered by anemoside B4 in the TNBS-induced rats. These proteins mainly clustered in tricarboxylic acid (TCA) cycle and respiratory electron transport chain. Among the altered proteins, S100A9 is one of the most significantly down-regulated proteins and associated with NF-κB and MAPK signaling pathways in the pathogenesis of UC. Further experiments revealed that anemoside B4 suppressed the expression of S100A9 and its downstream genes including TLR4 and NF-κB in colon. In vitro, anemoside B4 could inhibit the NF-κB signaling pathway induced by recombinant S100A9 protein in human intestinal epithelial Caco-2 cells. Moreover, anemoside B4 inhibits neutrophils recruitment and activation in colon induced by TNBS. Conclusions Our results demonstrate that anemoside B4 prevents TNBS-induced colitis by inhibiting the NF-κB signaling pathway through deactivating S100A9, suggesting that anemoside B4 is a promising therapeutic candidate for colitis.

Syringin protects against cerebral ischemia/reperfusion injury via inhibiting neuroinflammation and TLR4 signaling

Perfusion ◽  
2021 ◽  
pp. 026765912110070
Author(s):  
Yan Liu ◽  
Xuyao Zhu ◽  
Xiuxia Tong ◽  
Ziqiang Tan
Keyword(s):  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Learning And Memory ◽  
Ischemia Reperfusion Injury ◽  
Neuroprotective Effect ◽  
Ischemia Reperfusion ◽  
Cerebral Damage ◽  
Memory Ability ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury

Introduction: Cerebral ischemia/reperfusion injury (CI/R) is associated with high mortality and remains a large challenge in the clinic. Syringin is a bioactive compound with anti-inflammation, antioxidant, as well as neuroprotective effects. Nevertheless, whether syringin could protect against CI/R injury and its potential mechanism was still unclear. Methods: Rats were randomly divided into five groups: sham group, syringin group, CI/R group, CI/R + syringin group, and CI/R + syringin + LPS (TLR4 agonist) group. The CI/R injury rat model was established by the middle cerebral artery occlusion (MCAO). The learning and memory ability of rats was estimated by the Morris water maze test. Modified neurological severity score test (mNSS) and infarct volume were detected to assess the neuroprotective effect of syringin. ELISA and RT-qPCR were used to analyze the concentration of proinflammation cytokines and the expression of TLR4. Results: CI/R injury induced increased mNSS scores and decreased learning and memory ability of rats. Syringin could significantly protect against CI/R injury as it decreased the cerebral damage and improved the cognitive ability of CI/R rats. Moreover, syringin also reduced neuroinflammation of CI/R injury rats. Additionally, TLR4 was significantly upregulated in CI/R injury rats, which was suppressed by syringin. The activation of TLR4 reversed the neuroprotective effect of syringin in CI/R rats. Conclusion: Syringin decreased the inflammation reaction and cerebral damage in CI/R injury rats. The neuroprotective effect of syringin may be correlated with the inhibition of TLR4.

Effects of cannabinoid and vanilloid receptor agonists and their interaction on learning and memory in rats

2017 ◽  
Vol 95 (4) ◽  
pp. 382-387 ◽  
Author(s):  
Mariam Shiri ◽  
Alireza Komaki ◽  
Shahrbanoo Oryan ◽  
Masoumeh Taheri ◽  
Hamidreza Komaki ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Cannabinoid Receptor ◽  
Vanilloid Receptor ◽  
Interactive Effects ◽  
Control Group ◽  
Acute Administration ◽  
Male Wistar Rats ◽  
Agonistic Effect ◽  
Stimulation Of

Despite previous findings on the effects of cannabinoid and vanilloid systems on learning and memory, the effects of the combined stimulation of these 2 systems on learning and memory have not been studied. Therefore, in this study, we tested the interactive effects of cannabinoid and vanilloid systems on learning and memory in rats by using passive avoidance learning (PAL) tests. Forty male Wistar rats were divided into the following 4 groups: (1) control (DMSO+saline), (2) WIN55,212–2, (3) capsaicin, and (4) WIN55,212–2 + capsaicin. On test day, capsaicin, a vanilloid receptor type 1 (TRPV1) agonist, or WIN55,212–2, a cannabinoid receptor (CB1/CB2) agonist, or both substances were injected intraperitoneally. Compared to the control group, the group treated with capsaicin (TRPV1 agonist) had better scores in the PAL acquisition and retention test, whereas treatment with WIN55,212–2 (CB1/CB2 agonist) decreased the test scores. Capsaicin partly reduced the effects of WIN55,212–2 on PAL and memory. We conclude that the acute administration of a TRPV1 agonist improves the rats’ cognitive performance in PAL tasks and that a vanilloid-related mechanism may underlie the agonistic effect of WIN55,212–2 on learning and memory.

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